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14. Cover Image, Volume 92, Number 10, October 2020

Author

Musarrat, Farhana, primary, Chouljenko, Vladimir, additional, Dahal, Achyut, additional, Nabi, Rafiq, additional, Chouljenko, Tamara, additional, Jois, Seetharama D., additional, and Kousoulas, Konstantin G., additional

Published
2020
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18. Peptides and peptidomimetics as therapeutic agents for Covid‐19.

Author

Dahal, Achyut, Sonju, Jafrin Jobayer, Kousoulas, Konstantin G., and Jois, Seetharama D.

Subjects
*SARS-CoV-2, *PEPTIDOMIMETICS, *PEPTIDES, *COVID-19, *VIRAL envelope proteins, *VIRAL proteins
Abstract

The severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) Covid‐19 pandemic has caused high morbidity and mortality rates worldwide. Virus entry into cells can be blocked using several strategies, including inhibition of protein‐protein interactions (PPIs) between the viral spike glycoprotein and cellular receptors, as well as blocking of spike protein conformational changes that are required for cleavage/activation and fusogenicity. The spike‐mediated viral attachment and entry into cells via fusion of the viral envelope with cellular membranes involve PPIs mediated by short peptide fragments exhibiting particular secondary structures. Thus, peptides that can inhibit these PPIs may be used as potential antiviral agents preventing virus entry and spread. This review is focused on peptides and peptidomimetics as PPI modulators and protease inhibitors against SARS‐CoV‐2. [ABSTRACT FROM AUTHOR]

Published
2022
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19. Synthesis, Characterization, and Evaluation of Near-IR Boron Dipyrromethene Bioconjugates for Labeling of Adenocarcinomas by Selectively Targeting the Epidermal Growth Factor Receptor

Author

Kaufman, Nichole E. M., primary, Meng, Qianli, additional, Griffin, Kaitlin E., additional, Singh, Sitanshu S., additional, Dahal, Achyut, additional, Zhou, Zehua, additional, Fronczek, Frank R., additional, Mathis, J. Michael, additional, Jois, Seetharama D., additional, and Vicente, M. Graça H., additional

Published
2019
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20. Modulation of co‐stimulatory signal from CD2–CD58 proteins by a grafted peptide.

Author

Parajuli, Pravin, Sable, Rushikesh, Shrestha, Leeza, Dahal, Achyut, Gauthier, Ted, Taneja, Veena, and Jois, Seetharama

Subjects
SURFACE plasmon resonance, AMINO acid residues, TRYPSIN inhibitors, TRYPSIN, CARRIER proteins, CELL adhesion, PROTEIN-protein interactions
Abstract

Peptides were designed to inhibit the protein–protein interaction of CD2 and CD58 to modulate the immune response. This work involved the design and synthesis of eight different peptides by replacing each amino acid residue in peptide 6 with alanine as well as grafting the peptide to the sunflower trypsin‐inhibitor framework. From the alanine scanning studies, mutation at position 2 of the peptide was shown to result in increased potency to inhibit cell adhesion interactions. The most potent peptide from the alanine scanning was further studied for its detailed three‐dimensional structure and binding to CD58 protein using surface plasmon resonance and flow cytometry. This peptide was used to graft to the sunflower trypsin inhibitor to improve the stability of the peptide. The grafted peptide, SFTI‐a1, was further studied for its potency as well as its thermal, chemical, and enzymatic stability. The grafted peptide exhibited improved activity compared to our previously grafted peptide and was stable against thermal and enzymatic degradation. [ABSTRACT FROM AUTHOR]

Published
2021
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21. Genotype Driven Therapy for Non-Small Cell Lung Cancer: Resistance, Pan Inhibitors and Immunotherapy

Author

Singh, Sitanshu S., Dahal, Achyut, Shrestha, Leeza, and Jois, Seetharama D.

Abstract

Eighty-five percent of patients with lung cancer present with Non-small Cell Lung Cancer (NSCLC). Targeted therapy approaches are promising treatments for lung cancer. However, despite the development of targeted therapies using Tyrosine Kinase Inhibitors (TKI) as well as monoclonal antibodies, the five-year relative survival rate for lung cancer patients is still only 18%, and patients inevitably become resistant to therapy. Mutations in Kirsten Ras Sarcoma viral homolog (KRAS) and epidermal growth factor receptor (EGFR) are the two most common genetic events in lung adenocarcinoma; they account for 25% and 20% of cases, respectively. Anaplastic Lymphoma Kinase (ALK) is a transmembrane receptor tyrosine kinase, and ALK rearrangements are responsible for 3-7% of NSCLC, predominantly of the adenocarcinoma subtype, and occur in a mutually exclusive manner with KRAS and EGFR mutations. Among drug-resistant NSCLC patients, nearly half exhibit the T790M mutation in exon 20 of EGFR. This review focuses on some basic aspects of molecules involved in NSCLC, the development of resistance to treatments in NSCLC, and advances in lung cancer therapy in the past ten years. Some recent developments such as PD-1-PD-L1 checkpoint-based immunotherapy for NSCLC are also covered.

Published
2020
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